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Background: Recent research has unveiled that approximately 50%-70% of patients afflicted with lung cancer also receive concurrent diagnoses of lung infections, most notably pneumonia. Among the critical multidrug-resistant pathogens frequently isolated from pneumonia-afflicted patients, Pseudomonas aeruginosa and Acinetobacter baumannii stand prominent. Here, we assessed the impact of antibiotics and vitamins on the lung cancer infection cell culture. Methods: The study delves into the antimicrobial properties of vitamins P, K, and E against A. baumannii and P. aeruginosa, employing the minimum inhibitory concentration method and scrutinizing biofilm formation within the A549 cell culture. Results: The combined application of vitamins and antibiotics exhibited a statistically significant effect on both the minimal inhibitory concentration values and biofilm formation (P < .05). Within the realm of fat-soluble vitamins, vitamins K and E, when integrated with antibiotics, revealed varying degrees of influence, with vitamin K displaying the most substantial fractional inhibitory concentration value. Vitamin E, on the other hand, demonstrated a comparatively weaker fractional inhibitory concentration than the other constituents. Nevertheless, it exhibited robust optical density and a pronounced capacity to inhibit biofilm formation. Moreover, among the vitamin groups, it is evident that vitamin E surpasses the efficacy of others (antibacterials affecting K < P < E). The collective application of all vitamins manifested the most potent fractional inhibitory concentration. Conclusion: The synergistic effects of vitamins with antibiotics, as evidenced in this study, may offer a promising alternative for treating multidrug-resistant A. baumannii and P. aeruginosa, subject to further investigation through molecular studies.

Despite efforts to find effective drugs for sepsis-associated acute kidney injury (SA-AKI), mortality rates in patients with SA-AKI have not decreased. Our study evaluated the protective effects of isoflavone osajin (OSJ) on SA-AKI in rats by targeting inflammation, oxidative stress, and apoptosis, which represent the cornerstones in the pathophysiological mechanism of SA-AKI. Polymicrobial sepsis was induced in rats via the cecal ligation and puncture (CLP) technique. Markers of oxidative stress were evaluated in kidney tissues using biochemical methods. The expression of interleukin-33 (IL-33), 8-hydroxydeoxyguanosine (8-OHdG), caspase-3, and kidney injury molecule-1 (KIM-1) was evaluated as indicators of inflammation, DNA damage, apoptosis, and SA-AKI respectively in the kidney tissues using immunohistochemical and immunofluorescent detection methods. The CLP technique significantly (p

ABSTRACTThis mixed-method study aims to determine the effect of the use of mobile virtual patient application with narrated case-based virtual patients as an assistive technology on students’ clinical reasoning skills. It makes a notable contribution by exploring the impact of mobile virtual patient applications on healthcare students’ clinical skills and their preparation for real-world patient care. In addition, the accuracy of the analysis results regarding the effect on student achievement was analyzed with a second dataset tool, and thus, aiming to increase reliability by verifying the same research question with a different quantitative analysis technique. In the qualitative part of the study, students’ views on the implementation were collected through an open-ended questionnaire and the data were subjected to content analysis. An achievement test was also developed to determine the development of students’ clinical reasoning skills, which revealed that each of the learning environments had different outcomes regarding students’ achievement and that supporting the traditional environment with the mobile virtual patient application yielded better results for increasing students’ achievement. Students’ opinions about the mobile virtual patient application and the process also support the increase in academic achievement aimed at measuring clinical reasoning skills. The content analysis showed that the students, who generally reported multiple positive factors related to the application, thought that the stories and cases presented created a perception of reality, and they especially highlighted the contribution of the application to learning the story organization. Based on all these results, it can be said that the application supports clinical reasoning, provides practical experience, improves academic achievement, and contributes positively to motivation.

This study was conducted to evaluate the protective impacts of green tea extract (GT) against cypermethrin-induced (CYP) neurotoxicity parameters such as acetylcholinesterase activity, oxidative stress, immune response, histopathology, apoptosis, and DNA damage in the brain tissues of rainbow trout (Oncorhynchus mykiss). The trial was divided into four groups (group 1, 2, 3 and 4). Group 1 was the control, while group 2 was treated with 0.1 mg/l of CYP, group 3 was treated with 0.1 mg/l of CYP + 100 mg/l of GT and group 4 was treated with 0.1 mg/l of CYP + 200 mg/l of GT for 14 days. While the level of malondialdehyde increased, the exposure to CYP in group 2 resulted in a reduction in acetylcholinesterase, lysozyme, total immunoglobulin, white blood cell, superoxide dismutase, and catalase levels in the brain tissues, as compared to group 1. Furthermore, CYP exposure in group 2 resulted in severe hyperaemia in meningeal and parenchymal vessels, accompanied by significant degeneration and necrosis. In addition, neurons in group 2 exhibited pronounced cytoplasmic expressions of 8-OHdG and caspase-3. On the contrary, both doses of 100 mg/l and 200 mg/l of GT demonstrated remarkable neuroprotective impacts against CYP toxicity across all parameters as mentioned above. In summary, this study conclusively showed that the administration of 200 mg dose of GT yielded more pronounced neuroprotective impacts, surpassing the impacts observed with the 100 mg dose of GT. The higher dosage effectively reduced CYP-induced oxidative stress, apoptosis and DNA damage, while exhibiting an enhanced immune response.

Objective(s): Cadmium (CD) causes widespread and severe toxic effects on various tissues. Studies have shown that apoptosis, inflammation, and endoplasmic reticulum stress play a role in organ damage caused by CD. Phenolic compounds with strong antioxidant effects are found in various fruits and vegetables. One of these compounds is Gallic acid (GA), which is found both free and hydrolyzable in grapes, pomegranate, tea, hops, and oak bark. Result of various studies show that GA has active antioxidant, anti-inflammatory, and anti-apoptotic properties. In our study, we investigated the mechanism of the protective effect of GA on CD-induced hepatotoxicity in rats. Materials and Methods: In this study, 50 adult male Sprague Dawley rats weighing approximately 200–250 g were used and the rats were divided into 5 groups: Control, CD, GA50+CD, GA100+CD, and GA100. The rats were treated with GA (50 and 100 mg/kg body weight), and Cd (6.5 mg/kg) was administrated to the rats for 5 consecutive days. The liver enzymes, TB levels in serum samples, oxidative stress, inflammation, ER stresses, apoptosis marker, histopathology, 8-OHDG, and caspase-3 positivity were analyzed. Results: CD administration significantly increased liver enzyme levels (AST, ALT, ALP, and LDH), MDA, IL-1-β, IFN-γ, TNF-α, IL-10, IL-6, GRP78, CHOP, ATF6, p -IRE1, sXBP, Bax mRNA expression, Caspase 3, and 8-OHdG expression (P

Abstract This study investigated the cytotoxic effects of oxidative stress (OS), high mobility group box 1 (HMGB1), ADAMTS (A disintegrin and metalloproteinase with thrombospondin motifs), and neuropathology associated with coenurus cerebralis (Taenia multiceps). ADAMTS-13, HMGB1, glutathione reductase (GR), copper/zinc superoxide dismutase (Cu/Zn SOD), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) expression levels were studied. The study found that ADAMTS-13 (P

INTRODUCTION: Osteoporosis is an important health problem and there is no effective treatment yet. phosphodiesterase 5 inhibitors are promising agents for the treatment of osteoporosis. In this study, we aimed to determine the effects of phosphodiesterase 5 inhibitors (vardenafil, tadalafil, and udenafil) on bone morphogenic protein-2 and 9 (BMP-2 and 9), vascular endothelial growth factor (VEGF), and oxidative stress markers (malondialdehyde and CoQ10) in liver tissue of rats with ovariectomy-induced osteoporosis. METHODS: 50 Albino wistar female rats were randomly divided into 5 groups of 10 rats per group. Groups were the sham-operated, ovariectomise (OVEX), OVEX + Tadalafil, OVEX + udenafil and OVEX + vardenafil, respectively. VEGF, BMP-2 and 9 levels were measured by ELISA kits. To detect levels of MDA and CoQ10, we used high pressure liquid chromatography method. RESULTS: The levels of VEGF, BMP-2 and 9 levels in the groups that applied PDE-5 inhibitors were significantly higher than in the sham and OVEX groups. There was no significant difference between the OVEX+vardenafil and OVEX+udenafil groups in terms of VEGF, BMP-2 and 9 levels. The levels of MDA and CoQ10 were significantly lower in the groups that applied PDE5 inhibitors than in the OVEX group. When the histological and immunohistochemical results were examined, it was seen that angiogenesis was significantly higher in PDE-5 inhibitor groups. DISCUSSION AND CONCLUSION: In conclusion, we can say that these inhibitors may have positi ve effects on bone mineralization and remodelling by inducing the expression of VEGF, BMP-2 and 9 in liver tissue.

This paper aimed to examine the impact of flavonoid osajin (OSJ) on liver damage induced by sepsis. A total of 30 male rats were divided into 5 groups (Sham, sepsis, OSJ 150, OSJ 300 and reference). During sepsis, elevated lipid peroxidation (LPO) level and catalase activity (CAT) and decreased glutathione (GSH) level and superoxide dismutase (SOD) activity were observed in hepatic tissues of sepsis group in comparison with Sham group. A strong interleukin-33 and caspase-3 expressions were detected in hepatic tissues of sepsis group. On the contrary, OSJ administration to OSJ 300 group showed a significant decrease (P < 0.001) in LPO level (176±2.926) and significant increase (P < 0.001) in GSH level (10.586±0.083) and SOD activity (29.152±0.094) in comparison with sepsis group (185.777±1.735, 8.246±0.124, 24.307±0.379 respectively). In addition, the consumption of OSJ reduced expressions of interleukin-33 and caspase-3 and improved histopathological integrity. In conclusions, OSJ has hepatoprotective effect against sepsis-induced liver injury.

Background: Mitochondrial dysfunction and metabolic abnormalities are acknowledged as significant factors in the onset of neurodegenerative disorders such as Parkinson’s disease (PD) and Alzheimer’s disease (AD). Our research has demonstrated that the use of combined metabolic activators (CMA) may alleviate metabolic dysfunctions and stimulate mitochondrial metabolism. Therefore, the use of CMA could potentially be an effective therapeutic strategy to slow down or halt the progression of PD and AD. CMAs include substances such as the glutathione precursors (L-serine and N-acetyl cysteine), the NAD+ precursor (nicotinamide riboside), and L-carnitine tartrate. Methods: Here, we tested the effect of two different formulations, including CMA1 (nicotinamide riboside, L-serine, N-acetyl cysteine, L-carnitine tartrate), and CMA2 (nicotinamide, L-serine, N-acetyl cysteine, L-carnitine tartrate), as well as their individual components, on the animal models of AD and PD. We assessed the brain and liver tissues for pathological changes and immunohistochemical markers. Additionally, in the case of PD, we performed behavioral tests and measured responses to apomorphine-induced rotations. Findings: Histological analysis showed that the administration of both CMA1 and CMA2 formulations led to improvements in hyperemia, degeneration, and necrosis in neurons for both AD and PD models. Moreover, the administration of CMA2 showed a superior effect compared to CMA1. This was further corroborated by immunohistochemical data, which indicated a reduction in immunoreactivity in the neurons. Additionally, notable metabolic enhancements in liver tissues were observed using both formulations. In PD rat models, the administration of both formulations positively influenced the behavioral functions of the animals. Interpretation: Our findings suggest that the administration of both CMA1 and CMA2 markedly enhanced metabolic and behavioral outcomes, aligning with neuro-histological observations. These findings underscore the promise of CMA2 administration as an effective therapeutic strategy for enhancing metabolic parameters and cognitive function in AD and PD patients.

Objective: To investigate the effects of melatonin on renal inflammation, oxidative stress, apoptosis, as well as DNA and tissue damage in acrylamide-induced nephrotoxicity in rats. Methods: Fifty male rats were randomly divided into five groups. The control group received distilled water by gastric lavage for 11 days and the acrylamide group was administered acrylamide (50 mg/kg, i.g.) for 11 days. The MEL10+ACR and MEL20+ACR groups received intraperitoneal melatonin 10 and 20 mg/kg, respectively, for 11 days, and acrylamide (50 mg/kg, i.g.) was administered 1 h after melatonin injection. The MEL20 group was injected with melatonin (20 mg/kg) for 11 days. Kidney function tests were performed and biochemical and inflammatory parameters were determined. In addition, histopathological, immunohistochemical, and immunofluorescence examinationswerecarried out. Results: Melatonin significantly abated acrylamide-induced rise in serum urea and creatinine levels. Acrylamide caused oxidative stress, inflammation, apoptosis, as well as DNA and tissue damage in the kidneys. Melatonin treatment alleviated acrylamide-induced renal damage by exhibiting antioxidant, anti-inflammatory, and anti- apoptotic effects. Moreover, melatonin significantly ameliorated acrylamide-caused histopathological changes in kidney tissue. Conclusions: Melatonin attenuates acrylamide-induced renal oxidative stress, inflammation, apoptosis, and DNA damage in rats.

INTRODUCTION: It was aimed to investigate the effect of topical boric acid on healing in the treatment of keratitis. METHODS: Keratitis was created by randomly 32 of 56 healthy rats with inoculating pseudomonas aeruginosa (1x108 colony-forming units/ml 0.05 ml of solution containing pseudomonas eruginosa-PA-ATC27853) by creating epithelial defects in the corneas and randomly distributed to 4 groups. The remaining 24 healthy rats were randomly divided into 3 groups, so that; group 1 (control group), group 2 (with pseudomonas keratitis), group 3 (with pseudomonas keratitis and 4% boric acid treatment), group 4 (with pseudomonas keratitis and 8% boric acid treatment), group 5 (with pseudomonas keratitis and vancomycin+ ceftazidime given), group 6 (non-keratitis and only 4% boric acid applied), group 7 (non-keratitis and only 8% boric acid applied). At the end of the study, the ocular tissues of the rats were removed and examined histopathologically. RESULTS: A clinically significant reduction in inflammation was detected in the groups using topical boric acid (p˂0,05). Decreased TGF-β1 staining was detected in the groups in which keratitis + %4 and %8 boric acid was treated topically (p˂0,05). Compared to the infected group (group 2), 4% and 8% boric acid administered groups revealed mild/moderate corneal edema and thickening, degeneration of the corneal epithelium, and mild/moderate inflammation in the interstitial (p˂0,05). DISCUSSION AND CONCLUSION: Topical boric acid drops may be an important therapeutic factor in tissue healing and in the fight against inflammation in the treatment of keratitis.

Abstract Background Alzheimer’s disease (AD) is associated with metabolic abnormalities linked to critical elements of neurodegeneration. We recently administered combined metabolic activators (CMA) to the AD rat model and observed that CMA improves the AD-associated histological parameters in the animals. CMA promotes mitochondrial fatty acid uptake from the cytosol, facilitates fatty acid oxidation in the mitochondria, and alleviates oxidative stress. Methods Here, we designed a randomised, double-blinded, placebo-controlled phase-II clinical trial and studied the effect of CMA administration on the global metabolism of AD patients. One-dose CMA included 12.35 g L-serine (61.75%), 1 g nicotinamide riboside (5%), 2.55 g N-acetyl-L-cysteine (12.75%), and 3.73 g L-carnitine tartrate (18.65%). AD patients received one dose of CMA or placebo daily during the first 28 days and twice daily between day 28 and day 84. The primary endpoint was the difference in the cognitive function and daily living activity scores between the placebo and the treatment arms. The secondary aim of this study was to evaluate the safety and tolerability of CMA. A comprehensive plasma metabolome and proteome analysis was also performed to evaluate the efficacy of the CMA in AD patients. Results We showed a significant decrease of AD Assessment Scale-cognitive subscale (ADAS-Cog) score on day 84 vs day 0 (P = 0.00001, 29% improvement) in the CMA group. Moreover, there was a significant decline (P = 0.0073) in ADAS-Cog scores (improvement of cognitive functions) in the CMA compared to the placebo group in patients with higher ADAS-Cog scores. Improved cognitive functions in AD patients were supported by the relevant alterations in the hippocampal volumes and cortical thickness based on imaging analysis. Moreover, the plasma levels of proteins and metabolites associated with NAD + and glutathione metabolism were significantly improved after CMA treatment. Conclusion Our results indicate that treatment of AD patients with CMA can lead to enhanced cognitive functions and improved clinical parameters associated with phenomics, metabolomics, proteomics and imaging analysis. Trial registration ClinicalTrials.gov NCT04044131 Registered 17 July 2019, https://clinicaltrials.gov/ct2/show/NCT04044131

Purpose: Chronic otitis media (COM) is one of the common infectious diseases of the middle ear caused by bacterial or viral pathogens. The purpose of the present study was to investigate the efficacy of boric acid (BA) in the treatment of COM by comparing topical 4% and 8% BA applications with systemic ciprofloxacin in a Pseudomonas aeruginosa (P. aeruginosa) inoculation-induced model of COM in rats. Materials and Methods: Forty-two Sprague Dawley rats were divided into seven equal groups. The COM model was created with P. aeruginosa. Clinical, histopathological and, immunohistochemical comparisons were performed between the control, COM, topical 4% and 8% BA treatment, a systemic ciprofloxacin treatment, and topical 4% and 8% BA contact groups. Results: In the COM model, moderate edema, inflammation, degeneration and moderate tumor necrosis factor-alpha (TNF-α) expression were detected with the application of 4% BA. Mild edema, inflammation, degeneration, and mild TNF-α expression were detected with 8% BA application. Conclusion: Both 4% and 8% BA treatment provided significant clinical, histopathological and immunohistochemical improvement. The application of 8% BA was found to exhibit greater therapeutic efficacy, with no harmful effect on the middle ear mucosa.

Sambucus nigra (SN) berry extract is characterized by high antioxidant and anti-inflammatory activity. The current study aimed to investigate the effect of SN berry extract against indomethacin (IND)-induced gastric ulcer in rats and the mechanism involved. SN berry extract alleviated IND-induced gastric ulcers, as shown by assessing pathological manifestations in the gastric mucosa. These protective effects are attributed to attenuated oxidative damage to the gastric mucosa, correlated to increased activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), enhanced glutathione (GSH) levels, total antioxidant capacity (TAC), and upregulation of the Nrf2/HO-1 cascade. Moreover, oxidative stress markers, including malondialdehyde (MDA) and total oxidant status (TOS), were downregulated in SN-extract-treated animals. Furthermore, SN berry extract suppressed gastric mucosal inflammation by downregulating interleukin (IL)-33, IL-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) levels, and attenuating myeloperoxidase (MPO) activity. The protective effects of SN berry extract were similar to those exerted by esomeprazole (ESO), an acid-secretion-suppressive drug. In conclusion, SN berry extract has antiulcerative effects, alleviating oxidative stress and inflammation.

Background/Aims Sepsis is an uncontrolled systemic infection, withcomplex pathophysiology that may result in acute lung organ damage and cause multiple organ failure. Although much research has been conducted to illuminate sepsis’s complex pathophysiology, sepsis treatment protocols are limited, and sepsis remains an important cause of mortality andmorbidity in intensive care units.Various studies have shown that idebenone (IDE) possesses strong antioxidant properties, which inhibit lipid peroxidation and protect cells from oxidative damage. The present study aimed to evaluate the protective effects of IDE against lung injury in a cecal ligation and puncture (CLP)-induced sepsis rat model. Methods Male albino Wistar rats were used. The animals were divided into a healthy control (no treatment), CLP, IDE control (200 mg/kg), and CLP + IDE subgroups (50 mg/kg, 100 mg/kg, and 200 mg/kg), with nine rats in each group.IDE was administered 1 h after CLP induction.To evaluate the protective effects of IDE, lung tissues were collected 16 h after sepsis for biochemical, immunohistochemical staining, and histopathological examination. Results IDE significantly ameliorated sepsis-induced disturbances in oxidative stress-related factors, with its effects increasing in accordance with the dose.IDE also abolished histopathological changes in lung tissues associated with CLP.Furthermore, interleukin 1 beta (IL-1β)and tumor necrosis factor-alpha (TNF-α) immunopositivity markedly decreased in the septic rats following IDE treatment. Conclusions IDE largely mitigated the inflammatory response in sepsis-induced lung injury by decreasing free radicals and preventing lipid peroxidation. The results suggest that IDE may represent a potential novel therapeutic drug for sepsis treatment.

Abstract Epidemiological studies suggest that acute kidney injury has certain effect on myocardial function. In this study, for the first time, we tested a boron compound namely lithium tetraborate an act as an anti-oxidant and anti-inflammatory agent in ischemia-reperfusion injury. For this, we employed an in vivo rat model with kidney ischemia reperfusion injury to evaluate cardiac injury to clarify the mechanisms of lithium tetraborate. The evaluation of cardiac injury through kidney artery occlusion and reperfusion rat model indicated that lithium tetraborate could (1) reduce oxidative stress-induced endothelial dysfunction; (2) attenuate the inflammatory response of cardiac cells; and (3) alleviate the apoptosis and necrosis of myocytes. In summary, lithium tetraborate demonstrates significant therapeutic properties that contribute to the amelioration of cardiac damage, and it could be a promising candidate for future applications in myocardial dysfunction.

Our study aimed to investigate effect of tocilizumab on the lung tissue in the presence of Acinetobacter baumannii infection in immunosuppressed rats. A forty-eight female Wistar albino rats were divided equally into eight groups: Group 1: Healthy (H), Group 2: Immunosuppressed (IM), Group 3: Healthy rats given A. baumannii bacteria (H+BAC), Group 4: Immunosuppressed rats given A. baumannii bacteria (IM+BAC), Group 5: Healthy rats given tocilizumab (H+TCZ), Group 6: Immunosuppressed rats given tocilizumab (IM+TCZ), Group 7: Healthy rats given A. baumannii bacteria and tocilizumab (H+BAC+TCZ), Group 8: Immunosuppressed rats given tocilizumab and A. baumannii bacteria (IM+BAC+TCZ). Fourteen days after the immunosuppression of group 2, 4, 6 and 8 with hydrocortisone, group 3, 4, 7 and 8 were A. baumannii was dropped into the trachea. One hour after A. baumannii application, TCZ was administered to Groups 5, 6, 7 and 8. NF-κB, IL-6 and NLRP3 mRNA expressions were decreased in the IM group compared to the healthy group (P

Abstract The purpose of this study was to evaluate the antifibrotic and antioxidant roles of theophylline (Theo), a bioactive compound, in bleomycin (BLM)-induced pulmonary fibrosis in Wistar albino rats. Assigned into 4 groups were 32 Wistar albino rats, comprising the control group (administered 0.9% isotonic saline), BLM group (treated with BLM at a dose of 2.5 mg/kg), BLM+Theo group (treated with Theo at a dose of 75 mg/kg + BLM at a dose of 2.5 mg/kg), and Theo group (treated with Theo at a dose of 75 mg/kg). In the BLM group, a significant decrease was observed in the catalase and glutathione peroxidase enzyme activities, and reduced glutathione (GSH) (p < 0.05, p< 0.05, p< 0.001, respectively), while the malondialdehyde (MDA) levels (p< 0.001) were significantly elevated when compared to the control group. However, the MDA levels in the BLM+Theo group were also significantly higher than in the control group (p< 0.01). Similarly, the GSH levels were significantly higher in the BLM+Theo group than in the BLM group (p< 0.05). The results indicated that Theo reduced the BLM-induced activation of nuclear factor-kappaB (NF-κB) and decreased interleukin-6 (IL-6) levels, together with significant amelioration of the immunohistochemical and histopathological architecture in the lung tissues. It was concluded that the administration of Theo had a positive effect on the GSH level, and activation of NF-κB and IL-6 expression, which were significant proinflammatory markers in the BLM-treated rats.

Evaluation is an essential component of the learning process when discerning learning situations. Assessing natural language responses, like short answers, takes time and effort. Artificial intelligence and natural language processing advancements have led to more studies on automatically grading short answers. In this review, we systematically analyze short-answer evaluation studies. We present the development of the field in terms of scientific production features, datasets, and automatic evaluation features. The field has developed with pioneering studies in the US. Researchers generally conduct applications with English datasets. There has been a significant increase in research in recent years with large language models that support many different languages. These models have applications that achieve accuracy close to that of human evaluators. In addition, deep learning models do not require traditional approaches' detailed preprocessing and feature engineering processes. The dataset size trend is 1000 and above regarding the number of responses. It was observed that metrics such as accuracy, precision, and F1 score were used in performance determination. It is seen that the majority of the studies focus on scoring or rating. In this context, there needs to be more literature on the context of evaluation system applications that can provide descriptive and formative feedback. In addition, the developed assessment systems must be actively used in learning environments.

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin and indomethacin (IND) are the most commonly prescribed for inflammation or pain. However, widespread use causes several adverse effects, such as gastric ulcers, upper gastric system bleeding, and erosions. Carnosic acid (CA) is an important natural antioxidant found in rosemary (Rosmarinus essentials) and exhibits a protective effect by suppressing oxidative stress and inflammation. This study aimed to investigate the impact of CA on IND-induced gastric ulceration. Wistar male rats received CA (100 mg/kg) or esomeprazole (ESP) (20 mg/kg, standard drug) by oral gavage for 14 days, after that gastric ulceration was induced by oral administration of 100 mg/kg IND. CA pretreatment attenuated both gross morphological lesions and histopathological alterations. CA strongly reduced IND-induced oxidative stress, verified by a decrease in MDA (p < 0.001) and TOS levels (p < 0.05). Furthermore, an IND-dependent increase in CAT (p < 0.001) and GPx (p < 0.01) activities, as well as a reduction in GSH levels (p < 0.01), were ameliorated by CA pretreatment. CA also attenuated inflammatory damage by suppressing IL-1β (p < 0.01), IL-6 (p < 0.01), and TNFα (p < 0.001) production and increasing Nrf2/HO-1 (p < 0.05) expressions. In conclusion, CA shows a gastroprotective effect by reducing oxidative stress and attenuating inflammation.

Objective(s): This study was designed to assess the effect of fraxin which has various biological properties against liver injury induced by cisplatin.Materials and Methods: In our study, 24 Wistar albino rats were randomly assigned to control, fraxin, cisplatin, and fraxin+cisplatin groups. Cisplatin 12 mg/kg IP and fraxin 40 mg/kg orally were applied. When the experiment ended, the rats were sacrificed and the liver tissues were taken rapidly. Liver tissue specimens were maintained under appropriate conditions. Later, biochemical, histopathological, and immunohistochemical evaluations were performed.Results: According to our biochemical findings, oxidant parameters increased while antioxidant parameters decreased in cisplatin group compared with control group. Antioxidant parameters increased but oxidant parameters decreased in fraxin + cisplatin group compared with the cisplatin group. Immunohistochemical evaluations showed that the expressions of TNF-α and Caspase-3 were negative in control and fraxin groups, whereas severe levels were found in the cisplatin group. However, it was determined that the expressions of TNF-α and Caspase-3 were in mild levels in fraxin + cisplatin treatment group. In addition, it was observed that the increase of pathological markers such as coagulation necrosis, hydropic degeneration, dilatation in sinusoid, and hyperemia in the cisplatin group were compatible with our biochemical and immunohistochemical findings. Conclusion: Biochemical, immunohistochemical, and histopathological results revealed that fraxin was effective in relieving cisplatin-induced liver damage.

Cyclophosphamide (CD) has a range of adverse effects on ovarian tissue in humans. It is widely an anticancer drug and used in autoimmune disorders. Also, CD produces reactive oxygen species. In the current study, we evaluated possible protective roles of Rhabdosciadium anatolyi (RA) and chlorogenic acid (CA) on histopathological alterations and immunohistochemical assessment of 8-OHdG in the ovarian tissues of female rats given cyclophosphamide. Female Wistar albino rats were divided into six experimental groups, each consisted of eight rats: control group, CD (200 mg/kg) with i.p. for the first day as single dose, CA (100 mg/kg), RA (300 mg/kg) for each day, RA (300 mg/kg) + CD (200 mg/kg) and CA(100 mg/kg) + CD (200 mg/kg) groups. The rats were administered treatments lasted 7 days for all groups. CA and RA treatment is associated with positive the ovary action CD-induced ovotoxicity in rats. CA and RA could ameliorate the histopathological and immunohistochemical finding restoring which may show moderate levels of primordial follicle, primary, secondary, tertiary and graafian follicles were observed degeneration in germinative cells. Therefore, our results suggest that chlorogenic acid and Rhabdosciadium anatolyi might be a protective effect for CD-induced ovotoxicity.

Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.

According to population-based studies, lung cancer is the prominent reason for cancer-related mortality worldwide in males and is also rising in females at an alarming rate. Sorafenib (SOR), which is approved for the treatment of hepatocellular carcinoma and renal cell carcinoma, is a multitargeted protein kinase inhibitor. Additionally, SOR is the subject of interest for preclinical and clinical trials in lung cancer. This study was designed to assess in vivo the possible effects of sorafenib (SOR) in diethylnitrosamine (DEN)-induced lung carcinogenesis and examine its probable mechanisms of action. A total of 30 adult male rats were divided into three groups (1) control, (2) DEN, and (3) DEN + SOR. The chemical induction of lung carcinogenesis was performed by injection of DEN intraperitoneally at 150 mg/kg once a week for two weeks. The DEN-administered rats were co-treated with SOR of 10 mg/kg by oral gavage for 42 alternate days. Serum and lung tissue samples were analyzed to determine SRY-box transcription factor 2 (SOX-2) levels. The tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) levels were measured in lung tissue supernatants. Lung sections were analyzed for cyclooxygenase-2 (COX-2) and c-Jun N-terminal kinase (JNK) histopathologically. In addition, cyclooxygenase-2 (COX-2) and c-Jun N-terminal kinase (JNK) were analyzed by immunohistochemistry and immunofluorescence methods, respectively. SOR reduced the level of SOX-2 that maintenance of cancer stemness and tumorigenicity, and TNF-α and IL-1β levels. Histopathological analysis demonstrated widespread inflammatory cell infiltration, disorganized alveolar structure, hyperemia in the vessels, and thickened alveolar walls in DEN-induced rats. The damage was markedly reduced upon SOR treatment. Further, immunohistochemical and immunofluorescence analysis also revealed increased expression of COX-2 and JNK expression in DEN-intoxicated rats. However, SOR treatment alleviated the expression of these inflammatory markers in DEN-induced lung carcinogenesis. These findings suggested that SOR inhibits DEN-induced lung precancerous lesions through decreased inflammation with concomitant in reduced SOX-2 levels, which enables the maintenance of cancer stem cell properties.

Liver pyruvate kinase (PKL) has recently emerged as a new target for non-alcoholic fatty liver disease (NAFLD), and inhibitors of this enzyme could represent a new therapeutic option. However, this breakthrough is complicated by selectivity issues since pyruvate kinase exists in four different isoforms. In this work, we report that ellagic acid (EA) and its derivatives, present in numerous fruits and vegetables, can inhibit PKL potently and selectively. Several polyphenolic analogues of EA were synthesized and tested to identify the chemical features responsible for the desired activity. Molecular modelling studies suggested that this inhibition is related to the stabilization of the PKL inactive state. This unique inhibition mechanism could potentially herald the development of new therapeutics for NAFLD.

Introduction: Ototoxicity refers to cellular damage or function impairment developing in the inner ear in association with any therapeutic agent or chemical substance, and still represents the principal side-effect restricting the use of cisplatin. Objective: The aim of this study was to perform a biochemical, functional and histopathological investigation of the potential protective effect of eugenol against cisplatin-induced ototoxicity. Methods: The study was performed with 24 female Sprague Dawley rats. Distortion product otoacoustic emissions tests were performed on all animals, which were randomized into four equal groups. A single intraperitoneal dose of 15 mg/kg cisplatin was administered to cisplatin group, while the eugenol group received 100 mg/kg eugenol intraperitoneal for five consecutive days. 100 mg/kg eugenol was administered to cisplatin + eugenol group for 5 days. On the third day, these rats were received a single dose of 15 mg/kg cisplatin. The control group was given 8 mL/kg/day intraperitoneal saline solution for five days. The distortion product otoacoustic emissions test was repeated 24 h after the final drug administration. All animals were sacrificed, and the cochleas were subsequently used for biochemical and histopathological examinations. Results: Cisplatin caused oxidative stress in the cochlea, impaired the cochlear structure and significantly reduced signal noise ratio levels. Administration of eugenol together with cisplatin reversed these effects and provided functional, biochemical and histopathological protection. Conclusion: The study findings represent the first indication in the literature that eugenol may protect against ototoxicity by raising levels of antioxidant enzymes and lowering those of oxidant parameters. Resumo: Introdução: A ototoxicidade refere-se ao dano celular ou comprometimento da função da orelha interna associado a qualquer agente terapêutico ou substância química e ainda representa o principal efeito colateral que restringe o uso da cisplatina. Objetivo: O objetivo deste estudo foi realizar uma investigação bioquímica, funcional e histopatológica do potencial efeito protetor do eugenol contra a ototoxicidade induzida pela cisplatina. Método: O estudo foi realizado com 24 ratos fêmeas Sprague Dawley. Testes de emissões otoacústicas por produto de distorção foram realizados em todos os animais, os quais foram randomizados em quatro grupos iguais. Uma única dose intraperitoneal de 15 mg/kg de cisplatina foi administrada ao grupo cisplatina, enquanto o grupo eugenol recebeu 100 mg/kg de eugenol intraperitoneal por cinco dias consecutivos. Foram administrados 100 mg/kg de eugenol ao grupo cisplatina + eugenol durante 5 dias. No terceiro dia, estes ratos receberam uma dose única de 15 mg/kg de cisplatina. O grupo controle recebeu 8 mL/kg/dia de solução salina intraperitoneal por cinco dias. O teste de emissões otoacústicas por produto de distorção foi repetido 24 horas após a administração final do medicamento. Todos os animais foram sacrificados e as cócleas foram posteriormente utilizadas para exames bioquímicos e histopatológicos. Resultados: A cisplatina causou estresse oxidativo na cóclea, prejudicou a estrutura coclear e reduziu significativamente os níveis da relação sinal/ruído. A administração de eugenol juntamente com a cisplatina reverteu esses efeitos e forneceu proteção funcional, bioquímica e histopatológica. Conclusão: Os achados do estudo representam a primeira indicação na literatura de que o eugenol pode proteger contra a ototoxicidade, eleva os níveis de enzimas antioxidantes e diminui os níveis dos parâmetros oxidantes. Keywords: Cisplatin-induced ototoxicity, Eugenol, DPOAE, Oxidative stress, 8-Hydroxy-2′-deoxyguanosine, Palavras-chave: Ototoxicidade induzida pela cisplatina, Eugenol, EOAPD, Estresse oxidativo, 8-Hidroxi-2′-deoxiguanosina

Introduction: Cisplatin is an antineoplastic agent widely used in the treatment of a variety of cancers. Ototoxicity is one of the main side-effects restricting the use of cisplatin. Objective: The purpose of this study was to investigate the protective efficacy of gallic acid, in biochemical, functional and histopathological terms, against ototoxicity induced by cisplatin. Methods: Twenty-eight female Sprague Dawley rats were included. Rats were randomly assigned into four groups of seven animals each. Cisplatin group received a single intraperitoneal dose of 15 mg/kg cisplatin. Gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days. Cisplatin + gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days and a single intraperitoneal dose of 15 mg/kg cisplatin at 3rd day. A control group received 1 mL intraperitoneal saline solution for five consecutive days. Prior to drug administration, all rats were exposed to the distortion product otoacoustic emissions test. The test was repeated on the 6th day of the study. All rats were then sacrificed; the cochleas were removed and set aside for biochemical and histopathological analyses. Results: In cisplatin group, Day 6 signal noise ratio values were significantly lower than those of the other groups. Also, malondialdehyde levels in cochlear tissues were significantly higher, superoxide dismutase and glutathione peroxidase activities were significantly lower compared to the control group. Histopathologic evaluation revealed erosion in the stria vascularis, degeneration and edema in the connective tissue layer in endothelial cells, impairment of outer hair cells and a decrease in the number of these calls. In the cisplatin + gallic acid group, this biochemical, histopathological and functional changes were reversed. Conclusion: In the light of our findings, we think that gallic acid may have played a protective role against cisplatin-induced ototoxicity in rats, as indicated by the distortion product otoacoustic emissions test results, biochemical findings and immunohistochemical analyses. Resumo: Introdução: A cisplatina é um agente antineoplásico amplamente usado no tratamento de vários tipos de câncer. A ototoxicidade é um dos principais efeitos colaterais que restringem o uso da cisplatina. Objetivo: O objetivo deste estudo foi investigar a eficácia protetora do ácido gálico, em termos bioquímicos, funcionais e histopatológicos, contra a ototoxicidade induzida por cisplatina. Método: Vinte e oito ratas Sprague-Dawley foram incluídas. As ratas foram distribuídas aleatoriamente em quatro grupos de sete animais cada. O grupo cisplatina recebeu uma única dose intraperitoneal de 15 mg/kg de cisplatina. O grupo ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos. O grupo cisplatina + ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos e uma única dose intraperitoneal de 15 mg/kg de cisplatina no terceiro dia. O grupo controle recebeu 1 mL de solução salina via intraperitoneal por cinco dias consecutivos. Antes da administração do fármaco, todos os ratos foram expostos ao teste de emissões otoacústicas - produto de distorção. O teste foi repetido no sexto dia do estudo. Todos os ratos foram então sacrificados; as cócleas foram removidas e reservadas para análises bioquímicas e histopatológicas. Resultados: No grupo cisplatina, os valores da relação sinal-ruído do dia 6 foram significativamente mais baixos aos dos outros grupos. Além disso, os níveis de malondialdeído nos tecidos cocleares foram significativamente mais altos, e as atividades de superóxido dismutase e glutatione peroxidase foram significativamente mais baixas em comparação com o grupo controle. A avaliação histopatológica revelou erosão na estria vascular, degeneração e edema na camada de tecido conjuntivo em células endoteliais, comprometimento das células ciliadas externas e diminuição do número dessas células. No grupo cisplatina + ácido gálico, estas alterações bioquímicas, histopatológicas e funcionais foram revertidas. Conclusão: Tendo em vista os nossos achados, consideramos que o ácido gálico pode ter desempenhado um papel protetor contra a ototoxicidade induzida por cisplatina em ratas, conforme indicado pelos resultados do teste emissões otoacústicas - produto de distorção, achados bioquímicos e análises imuno-histoquímicas. Keywords: Cisplatin-induced ototoxicity, Gallic acid, Oxidative stress, DPOAE, Palavras-chave: Ototoxicidade induzida por cisplatina, Ácido gálico, Estresse oxidativo, EOAPD

High-grade gliomas are the most fatal brain tumors. Grade 4 gliomas are called glioblastoma multiforme (GBM), which are associated with the poorest survival and a 5-year survival rate of less than 4%. Many patients with GBM developed concomitant cognitive dysfunctions and epilepsy. Although the cognitive decline is well defined in glioblastomas, the neurotoxic factors underlying this pathology are not well understood in GBM patients. In this study, we aimed to investigate whether GBM-derived exosomes play a role in neuronal toxicity. For this purpose, exosomes obtained from T98G and U373 GBM cells were applied to primary neuron culture at different concentrations. Subsequently, MTT, LDH, GSH, TAS, and TOS tests were performed. Both GBM-derived exosomes induced a dose-dependent and statistically significant increase of LDH release in cerebellar neurons. MTT assay revealed as both T98G and U373 GBM-derived exosomes induced dose-dependent neurotoxic effects in cerebellar neurons. To the best of our knowledge, this study is the first study demonstrating the toxic potential of GBM-derived exosomes to primary neurons, which may explain the peritumoral edema and cognitive decline in GBM patients.

Ototoxicity refers to cellular damage or functional disorder developing in the inner ear in association with any therapeutic agent or chemical substance. Cisplatin, one of these agents capable of causing ototoxicity, is a chemotherapeutic used in several malignancies. Ferulic acid (FA) is a phenolic acid with known anti-oxidative and anti-inflammatory properties. The purpose of this study was to perform a biochemical and histopathological investigation of the protective efficacy of FA against cisplatin-induced ototoxicity in rats. Twenty-four Wistar rats were used in this study. Animals were randomly assigned into four groups of six rats each. Rats in the control group received intraperitoneal injection of 1 ml salin for four consecutive days. Rats in the cisplatin group received a single intraperitoneal administration of 10 mg/kg cisplatin. Rats in the FA group received intraperitoneal FA at 100 mg/kg for four days, and rats in the cisplatin+FA group received intraperitoneal FA at 100 mg/kg 1 h after administration of intraperitoneal cisplatin at 10 mg/kg, this procedure being performed for four consecutive days. Rats were sacrificed 24 h after the final drug administration. Cochlear tissues were removed for biochemical and histopathological analysis. MDA levels were significantly higher in cochlear tissues of the rats receiving cisplatin compared to the control group. MDA levels in rats receiving cisplatin and treated with FA were significantly lower than those in the cisplatin group. Activities of SOD and GPx decreased significantly in the cochleas of rats administered cisplatin compared to the control group. Both SOD and GPx activities were significantly higher in rats administered FA and cisplatin in combination compared to the cisplatin only. Histopathological evaluation of cochleas of the rats revealed significant protection of FA against cisplatin induced ototoxicity. This study, the first in the literature, shows that FA exhibits a protective effect against cisplatin-induced ototoxicity. [Med-Science 2018; 7(3.000): 528-31]

Cis-diammineedichloroplatinum (cisplatin) is a chemotherapeutic agent used for the treatment of several types of cancer. However, severe side-effects such as ototoxicity, nephrotoxicity and neurotoxicity restrict its use. p-Coumaric acid (PCA) is a phenol class compound obtained from various plants in nature such as grape, carrot and tomato and from beverages such as tea and beer. It was shown to have antioxidant and free radical scavenging, anti-inflammatory and neuroprotective effects. The purpose of this study was to perform a biochemical and histopathological evaluation of the protective efficacy of PCA in ototoxicity induced with cisplatin in rats. To the best of our knowledge, no previous research has investigated the protective effect of PCA against cisplatin-induced ototoxicity. 28 Wistar rats were used. The animals were randomly divided into four groups of seven members each. No drug was administered to the rats in the control group, while the cisplatin group received a single intraperitoneal dose of 10 mg/kg cisplatin. PCA was administered to the PCA group rats by the intraperitoneal route for three days at a dose of 100 mg/kg. In the cisplatin+PCA group, intraperitoneal PCA at 100 mg/kg was administered one hour after injection of 10 mg/kg intraperitoneal cisplatin for three consecutive days. Rats were sacrificed 24 h after the final drug administration. The cochlear tissues were removed and MDA levels, GPx and SOD activities were measured to evaluate the oxidative stress status and histopathological evaluation was performed to reveal cochlear damage. The results showed that PCA protects the cochlea from ototoxic effect of cisplatin. PCA is a reliable agent that provides significant biochemical and histopathological protection against cisplatin-induced ototoxicity in rats. [Med-Science 2018; 7(2.000): 373-77]

Probiotics have been shown to have positive effects when it comes to combating various health issues when consumed, preventing even the absorption of environmental toxins. One of the main environmental toxins encountered today is pesticide residues. Neonicotinoids, widely applied today in countries that have approved of them, are a known class of insecticides with an excellent and effective potency. Neonicotinoids have been shown to cause various toxic effects, either acutely or chronically, on human health and on beneficial insects when exposed. To clarify the assumption that probiotics could counteract these toxic effects, especially on vital organs, the probiotic yeast “Saccharomyces boulardii” (S. boulardii) was tested against the neonicotinoids, acetamiprid (ACE) and imidacloprid (IMI), as it has outstanding physiological and metabolic properties. The results obtained from the studies indicated that although ACE and IMI induced liver, kidney, brain and bowel damage, there was a considerable level of protection by the dietary supplementation of S. boulardii, as it reduced the absorption of these insecticides.

The aim of this study was to investigate the effect of hesperidin on male reproductive system in rats to which methotrexate (MTX) was administered. In the study, 28 male Wistar albino rats at the age of 8 weeks and had 250-300 g of live weight were used. Four experimental groups were formed; Group 1 (n=7): The control group, only feed and water were given. Group 2 (n=7): MTX group, a single dose of 20 mg/ kg of i.p. MTX was administered. Group 3 (n=7): Hesperidin group, 200 mg/kg of hesperidin was administered by gavage for 7 days. Group 4: MTX + hesperidin group (n=7): Following administration of a single dose of 20 mg/kg i.p. MTX , 200 mg/kg of Hesperidin was administered by oral gavage for 7 days. At the end of the experiment, rats were decapitated and biochemical, histopathological and spermatological parameters were examined. It was observed that in the MTX group, sperm motility and density, the enzymes CAT, GPx and SOD and GSH level decreased, TNF-alpha and IL-1 Beta, as well as MDA, levels were increased, regular structure of spermatogenic cells was impaired, and seminiferous tubules became necrotic and degenerative. It was determined that spermatological parameters improved and, necrotic and degenerative changes diminished by the administration of MTX+hesperidin. These outcomes indicated that hesperidin had a protective effect on destructive effects of MTX in rat testiclesv.

Aujeszky"s disease, also known as pseudorabies, is caused by an alphaherpesvirus that infects the central nervous system and other system. Disease was first recognized as a fatal viral disease of cattle and dogs in 1902. The natural infections have been reported worldwide in swine, cattle, dogs and variety of wildlife species in more recent years. The study material was a 5 years old cow which was brought with symptoms such as skin itching, weakness, convulsions, fever and neurogical signs. As a result of the clinical examination the animal was suspected for Aujeszky"s disease. Slaughter and necropsy were recommended. Subsequent to necropsy, tissues were fixed in formalin. Samples were evaluated histopathologically and immunohistochemically. According to the histopathological findings; diffuse, nonsuppurative inflammation of brain, spinal cord and spinal nerves were determined. Brain lesions were detected commonly in cerebral and cerebellar cortexes. Grey and white matter were both affected. It was observed marked perivascular lymphoplasmocytic cell infiltration, glial cell proliferation, Hyperemia and hemoragia in veins in brain and light chromatolysis have been identified in some neurons. Intranuclear inclusions were observed in neurons. On the skin itching region of animal, serofibrinous inflammation in the dermis and subcutis was detected. According to the immunohistochemical findings; immunoperoxidase was detected strong positive in cytoplasms of both neurons and glial cells in areas with meningitis in brain. Consequently; after clinical, macroscopical and microscopical examination, this case was diagnosed as Aujeszky"s disease. The aim of this study is presenting this disease immunochemically as it has never been reported in cattle in Turkey. We believe that it would be appropriate to present this case report since it is the first Pseudorabies case in cattle in Turkey

Context: Ferulago angulata (Schlecht.) Boiss. (Apiaceae) (FASB) is used to treat liver diseases and has been used both as food and therapeutics by many cultures for thousands of years because of the natural antioxidant compounds. Objective: This study determines antioxidant properties of FASB flowers, the levels of minerals and vitamins, and also, evaluates the hepatoprotective effect of flowers against N-nitrosodimethylamine (NDMA) induced on liver tissue by assessing antioxidant enzymes and histopathological parameters in Wistar albino rats. Materials and methods: In the study, the rats were divided into six groups of ten. Control, untreated animals were given 0.9% NaCl. Rats were intraperitoneally given NDMA (10 mg/kg) for the first 7 days. FASB methanol extract (150 and 300 mg/kg) was administered orally for 21 days. Results: α-Tocopherol, retinol, ascorbic acid, total antioxidant activity, phenolic and flavonoid contents of FASB were 0.70 ± 0.13, 0.29 ± 0.03 μg/g, 139.32 ± 7.06 μg/100 g, 171.61 ± 6.05 mM ascorbic acid/g, 90.47 ± 4.11 mg GA/g and 37.39 ± 2.85 mg QE/g. DPPH and hydroxyl radical scavenging activity was obtained IC50 67.34 ± 4.14 and 64.87 ± 4.68 μg/mL, respectively. Discussion and conclusion: The results of the study indicated that FASB flowers contain high levels of vitamins, minerals, total antioxidant activity, phenolics and flavonoids. Due to the positive effect on significant changes in antioxidant enzymes of liver tissue and histopathological examination, it is thought that the plant could be used as a hepatoprotective.